Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease characterized by dysregulation of the immune system and differential expression of genes in immunological pathways. In the United States, SLE affects about 2 million patients and 90% of these patients are female. Targeted tissues and organs include the blood, central nervous system (CNS), joints, kidneys, lungs, skin, and vasculature, Symptoms include abnormal blood panels, arthralgias, atherosclerosis, CNS disorders, infections, joint pain, malaise, rashes, ulcers, and the production of autoantibodies. Since disease severity, symptomology, and response to therapy vary widely, SLE is difficult to diagnose, manage and treat.
As described in USSN 20040033498, SLE clearly involves differential gene expression in SLE patients as compared to normal controls. Two laboratories have reported on the role of the interferon (INF)-α inducible genes in SLE and on high levels of anti-RNA binding protein, anti-Ro antibodies, and renal disease (Baechler et al (2003) PNAS100:2610-2615; Kirou et al (2004) Arthritis and Rheumatism 50:3958-3967). However, low positive correlation between disease activity and IFN-inducible genes, the apparent heterogeneity of SLE patients, and lack of longitudinal studies continue to present challenges for clinicians (Kirou et al. (2005) Arthritis and Rheumatism 52:1491-1503).
These challenges point to a need in the art for better diagnosis, characterization, and follow-up of patients with SLE. To this end, longitudinal data from SLE patients was used with methods for detecting and analyzing gene expression to monitor status, quiescence versus flare, and to classify a patient as having type 1 SLE or type 2 SLE.